Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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Exudative retinal detachment

Pathogenesis

Exudative RD is characterized by the accumulation of SRF in the absence of retinal breaks or traction. It may occur in a variety of vascular, inflammatory and neoplastic diseases involving the NSR, RPE and choroid in which fluid leaks outside the vessels and accumulates under the retina. As long as the RPE is able to compensate by pumping the leaking fluid into the choroidal circulation, no fluid accumulates in the subretinal space and RD does not occur. However, when the normal RPE pump is overwhelmed, or if the RPE activity is decreased, then fluid starts to accumulate in the subretinal space. The main causes are the following:

1Choroidal tumours such as melanomas, haemangiomas and metastases; it is therefore very important to consider that exudative RD is caused by an intraocular tumour until proved otherwise.

2 Inflammation such as Harada disease and posterior scleritis.

3Bullous central serous chorioretinopathy is a rare cause.

4Iatrogenic causes include retinal detachment surgery and panretinal photocoagulation.

5 Subretinal neovascularization which may leak and give rise to extensive subretinal accumulation of fluid at the posterior pole. 6 Hypertensive choroidopathy, as may occur in toxaemia of pregnancy, is a very rare cause.

7Idiopathic such as the uveal effusion syndrome (see above).

Diagnosis

1Symptoms. Photopsia is absent because there is no vitreoretinal traction, although floaters may be present if there is associated vitritis. The visual field defect may develop suddenly and progress rapidly. Depending on the cause both eyes may be involved simultaneously (e.g. Harada disease).

2Signs

•The RD has a convex configuration, just like a rhegmatogenous RD, but its surface is smooth and not corrugated.

•The detached retina is very mobile and exhibits the phenomenon of ‘shifting fluid’ in which SRF responds to the force of gravity and detaches the area of retina under which it accumulates.

•For example, in the upright position the SRF collects under the inferior retina (Fig. 16.59A), but on assuming the supine position for several minutes, the inferior retina flattens and the SRF shifts posteriorly detaching the superior retina (Fig. 16.59B).

•The cause of the RD, such as a choroidal tumour (Fig. 16.60), may be apparent when the fundus is examined, or the patient may have an associated systemic disease responsible for the RD (e.g. Harada disease, toxaemia of pregnancy).

•‘Leopard spots’ consisting of scattered areas of subretinal clumping may be seen after the detachment has flattened (Fig. 16.61).

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Fig. 16.59 Exudative retinal detachment with shifting fluid. (A) Inferior collection of subretinal fluid with the patient sitting; (B) the subretinal fluid shifts upwards when the patient assumes the supine position

(Courtesy of CL Schepens, E Hartnett and T Hirose, from Schepens’ Retinal Detachment and Allied Diseases, Butterworth-Heinemann, 2000)

Fig. 16.60 Exudative retinal detachment caused by a choroidal melanoma

(Courtesy of B Damato)

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Fig. 16.61 ‘Leopard spot’ pigmentation following resolution of exudative retinal detachment

Treatment

Treatment depends on the cause. Some cases resolve spontaneously, whilst others are treated with systemic corticosteroids (Harada disease and posterior scleritis). In some eyes with bullous central serous chorioretinopathy, the leak in the RPE can be sealed by argon laser photocoagulation.

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Pars plana vitrectomy

Introduction

Instrumentation

The diameter of the shaft of most instruments is 0.9 mm (20-gauge); they are therefore interchangeable and can be inserted through either sclerotomy. Smaller 21g and 25g systems are becoming increasingly popular. These smaller sclerotomies do not usually require suturing but there is some concern that sealing occurs via vitreous incarceration with an increased risk of postoperative endophthalmitis.

1The cutter has an inner guillotine blade which oscillates at up to 1500 times/minute (Fig. 16.62 bottom), cutting the vitreous gel into tiny pieces and simultaneously removing it by suction into a collecting cassette. Newer high speed cutters (over 2500 oscillations per minute) are increasingly being used, exerting less traction on the vitreoretinal interface during surgery.

2The intraocular illumination source is through a 20-gauge fibreoptic probe (Fig. 16.62 top) which delivers light from an 80–150 W bulb. Brighter, high-intensity halogen-type light sources are also becoming available and can be inserted via a self-retaining cannula into a fourth port. These have the advantage of allowing the surgeon to carry out true bimanual surgery, which can be particularly useful in challenging cases such as advanced tractional diabetic retinal detachment.

3The infusion cannula usually has an intraocular length of 4 mm, although in special circumstances such as choroidal detachment or eyes with opaque media, a 6 mm cannula may be required.

4Accessory instruments include scissors, forceps, flute needle, and endodiathermy and endolaser delivery systems.

5Wide-angle viewing system (Fig. 16.63) consists of an indirect lens beneath the operating microscope and an incorporated series of prisms to reinvert the image. The field of view extends almost to the ora serrata; higher magnification lenses are also available for macular surgery.

Fig. 16.62 (Top) Illumination pipe; (bottom) cutter

(Courtesy of V Tanner)

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Fig. 16.63 Viewing systemfor pars plana vitrectomy

(Courtesy of V Tanner)

Tamponading agents

1Purpose is to achieve intraoperative retinal flattening by fluid–gas exchange combined with internal drainage of SRF, and to produce internal tamponade of retinal breaks during the postoperative period.

2Expanding gases. Although air can be used in certain cases, one of the following expanding gases is usually preferred in order to achieve prolonged intraocular tamponade:

•Sulphur hexafluoride (SF6), which doubles its volume if used at a 100% concentration and lasts 10–14 days.

•Perfluorethane (C2F6), which triples its volume at 100% and lasts 30–35 days.

•Perfluoropropane (C3F8), which quadruples its volume at 100% and lasts 55–65 days.

Because the eye is usually left almost entirely gas-filled at the end of the procedure, most tamponading agents are used at an isovolumetric concentration (e.g. 20–30% for SF6 and 12–16% for C3F8).

3Heavy liquids (perfluorocarbons) have a high specific gravity – they are heavier than water – and thus remain in a dependent position when injected into the vitreous cavity.

4Silicone oils have a low specific gravity and are thus buoyant. They allow for more controlled intra-operative retinal manipulation and may also be used for prolonged postoperative intraocular tamponade. The most commonly used liquid silicones have relatively low viscosity (1000–5000 cs). The 1000 cs silicone is easy to inject and to remove whilst 5000 cs silicone is less prone to the production of tiny droplets (emulsification).

5Long-term heavy liquid tamponade. Although primarily developed for intraoperative use, newer perfluorocarbon compounds are available for postoperative tamponade of the inferior retina. However, problems have been noted with retinal toxicity and potentially severe postoperative inflammation.

Indications

Although most simple rhegmatogenous RD can be treated successfully by scleral buckling techniques, vitrectomy surgery has greatly improved the prognosis for more complex detachments. As techniques have improved and surgeons’ familiarity and confidence has grown, the threshold for vitrectomy surgery has fallen. Many surgeons now feel that morbidity and success rates are better with vitrectomy for all pseudophakic and aphakic RD, and for those that would otherwise require drainage of SRF. The guidelines below are therefore not absolute but intended to give some insight into the factors influencing the decision-making process.

Rhegmatogenous retinal detachment

1In which retinal breaks cannot be visualized as a result of haemorrhage, vitreous debris, posterior capsular opacity, IOL edge effects. Vitrectomy is crucial to provide an adequate retinal view. Scleral buckling carries a high risk of failure if any breaks are missed.

2In which retinal breaks cannot be closed by scleral buckling such as giant tears (Fig. 16.64A), large posterior breaks (Fig. 16.64B) and PVR (Fig. 16.64C).

Fig. 16.64 Some indications for pars plana vitrectomy. (A) Giant retinal tear; (B) large posterior tear; (C) severe proliferative vitreoretinopathy; (D) tractional retinal detachment

(Courtesy of C Barry – figs A-C)

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Tractional retinal detachment

1Indications in diabetic RD

aTractional RD threatening or involving the macula (Fig. 16.64D). Vitrectomy is always combined with internal panretinal photocoagulation to prevent postoperative neovascularization that may cause vitreous haemorrhage or rubeosis iridis. Extramacular tractional RD may be observed without surgery because, in many cases, it remains stationary for a long time provided proliferative retinopathy has been controlled.

bCombined tractional-rhegmatogenous RD should be treated urgently, even if the macula is not involved, because SRF is likely to spread quickly.

2Indications in penetrating trauma

aPrevention of tractional RD. Unlike diabetic retinopathy where epiretinal membrane proliferation occurs mostly on the posterior retina, fibrocellular proliferation after penetrating trauma tends to develop on the pre-equatorial retina and/or the ciliary body. Treatment is usually aimed at visual rehabilitation and minimizing the tractional process.

bLate tractional RD, which may be associated with an intraocular foreign body or retinal incarceration, occasionally develops months after otherwise successful surgery.

Technique

Basic vitrectomy

aFollowing limbal peritomy an infusion cannula is secured to the sclera (3.5 mm behind the limbus in pseudophakic or aphakic eyes and 4 mm in phakic eyes) at the level of the inferior border of the lateral rectus muscle.

bFurther sclerotomies are made at the 10 and 2 o’clock positions. These can be standard stab incisions made with an MVR blade, or self-sealing sclerotomies.

c The cutter and fibreoptic light pipe enter through the upper two sclerotomies (Fig. 16.65).

dThe central vitreous gel and posterior hyaloid face are excised.

Fig. 16.65 Infusion cannula, light pipe and cutter in position (right eye)

The above basic steps apply to all vitrectomies although transconjunctival small gauge systems do not require a peritomy or postoperative suturing. Subsequent steps depend on the characteristics of the RD as follows.

Closure of giant tears

aFluid-air exchange is performed to flatten the retina (hydraulic retinal reattachment).

bThe flap of a giant tear is unrolled by injecting a heavy liquid over the optic disc (Fig. 16.66).

c Retinopexy of the now flat retinal breaks is performed with either trans-scleral cryotherapy or endolaser using minimal energy.

dProlonged internal tamponade is achieved by replacing air with a non-expansile concentration of sulphur hexafluoride (SF6) or perfluoropropane (C3F8) gases, or with silicone oil. The non-expansile mixture of gas and air is prepared in a large (50 mL) syringe and the air-filled vitreous cavity is flushed with 20% or 30% SF6–air mixture or 14–16% C3F8–air mixture.

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Fig. 16.66 Unrolled giant tear using heavy liquid

(Courtesy of C Barry)

Proliferative vitreoretinopathy

The aims of surgery in PVR are to release both transvitreal traction by vitrectomy and tangential (surface) traction by membrane dissection in order to restore retinal mobility and allow closure of retinal breaks.

aLocalized fixed retinal folds ('star folds’) may be freed by the removal of the central plaque of epiretinal membrane. This can usually be achieved by engaging the tip of the vertically cutting scissors (Fig. 16.67), or other pic-type instrument, in the edge of the valley of the membrane between two adjacent retinal folds. The membrane is then either surgically dissected or simply peeled from the surface of the retina.

bThe decision to perform a relieving retinotomy is made after epiretinal membrane dissection has been performed as completely as possible but retinal mobility is deemed insufficient for lasting re-attachment.

Fig. 16.67 Dissection of star folds with vertically cutting scissors in proliferative vitreoretinopathy

Tractional retinal detachment

The goal of vitrectomy in tractional RDs is to release anteroposterior and/or circumferential vitreoretinal traction. Because the membranes are vascularized, and the retina often friable, they cannot be simply peeled from the surface of the retina as this would result in haemorrhage and tearing of the retina. The two methods of removing fibrovascular membranes in diabetic tractional RDs are the following:

1Delamination involves the horizontal cutting of the individual vascular pegs connecting the membranes to the surface of the retina (Fig. 16.68). This is preferred to segmentation (see below) because it allows the complete removal of fibrovascular tissue from the retinal surface (en bloc delamination).

2Segmentation involves the vertical cutting of epiretinal membranes into small segments (Fig. 16.69). It is used to release circumferential vitreoretinal traction when delamination is difficult or impossible, such as in very mobile combined tractionalrhegmatogenous RD associated with posterior retinal breaks.

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Fig. 16.68 (A) Delamination with horizontally cutting scissors; (B) delamination completed

Fig. 16.69 (A) Segmentation with vertically cutting scissors; (B) segmentation completed

Postoperative complications

Raised intraocular pressure

Elevation of intraocular pressure may be caused by the following mechanisms:

1Overexpansion of intraocular gas may cause raised intraocular pressure as a result of complete filling of the vitreous cavity if the concentration of expansile gas used was inadvertently too high.

2Silicone oil-associated glaucoma

aEarly glaucoma may be caused by direct pupillary block by silicone oil (Fig. 16.70A). This occurs particularly in the aphakic eye with an intact iris diaphragm. In aphakic eyes this can be prevented by performing an inferior (Ando) iridotomy at the time of surgery to allow free passage of aqueous to the anterior chamber.

bLate glaucoma is caused by emulsified silicone in the anterior chamber (Fig. 16.70B) which causes trabecular blockage. The risk of this complication may be reduced by an early removal of silicone oil either via the pars plana in phakic eyes or the limbus in aphakic eyes, although late glaucoma can still occur even following prompt removal of apparently nonemulsified oil.

3 Other mechanisms include ghost cell and steroid-induced glaucoma (see Ch. 10).

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Fig. 16.70 Some complications of silicone oil injection. (A) Pupillary block glaucoma caused by oil in the anterior chamber; (B) late glaucoma due to trabecular blockage by emulsified oil; (C) cataract in an eye with emulsified oil (inverted ‘pseudo-hypopyon’); (D) band keratopathy

(Courtesy of Z Gregor – fig. D)

Cataract

Lens opacity may be caused by the following mechanisms:

1Gas-induced. The use of either a large and/or long-lasting intravitreal gas bubble almost invariably gives rise to feathering of the posterior subcapsular lens cortex; fortunately opacification is usually transient in these circumstances.

2Silicone-induced. Almost all phakic eyes with silicone oil eventually develop cataract (Fig. 16.70C). If a cataract forms, the silicone oil can be removed in conjunction with phacoemulsification, posterior capsulorhexis to allow release of oil and subsequent posterior chamber lens implantation.

3Delayed cataract formation. Following successful vitrectomy a large proportion of eyes develop nuclear sclerosis within 1 year if the patient is over 50 years of age.

Band keratopathy

Band keratopathy may occur as a result of prolonged contact between silicone oil and the corneal endothelium (Fig. 16.70D).

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Chapter 17 – Vitreous Opacities

Introduction 730 Muscae volitantes 730

Vitreous haemorrhage 730

Asteroid hyalosis (Benson disease) 730 Synchisis scintillans (cholesterolosis bulbi)  730

Amyloidosis 730 Vitreous cyst 733

Introduction

The vitreous is a transparent extracellular gel, with a complicated structural framework consisting of collagen, soluble proteins, hyaluronic acid and a water content of 99%. Its total volume is approximately 4.0 mL. The few cells normally present in the gel are located predominantly in the cortex and consist of hyalocytes, astrocytes and glial cells. The vitreous provides structural support to the globe while providing a clear path for light to reach the retina. It also hinders the forward diffusion of oxygen from the retinal blood supply to the anterior segment. Once liquefied or surgically removed it does not reform. Vitreous opacities may be caused by developmental abnormalities, trauma or disease. Most have already been described in other chapters (e.g. snowballs, malignant cells, parasitic cysts and hereditary vitreoretinopathies) and will not be mentioned here.

Muscae volitantes

Muscae volitantes are extremely common minute fly or worm-like physiological opacities best seen against a pale background. They are likely to predominently represent tiny embryological remnants in the vitreous gel.

Vitreous haemorrhage

Vitreous haemorrhage is a relatively common condition that has many diverse causes (Table 17.1), most of which have been described elsewhere in the book.

1The symptoms vary according to the severity of the bleed. Mild haemorrhage (Fig. 17.1A) causes sudden diffuse blurring of vision and floaters, but may not affect visual acuity, whilst a dense bleed may result in very severe visual loss.

2B-scan ultrasonography in unclotted vitreous haemorrhage generally shows a uniform medium grey appearance (Fig. 17.1C). Once cellular aggregates develop, small particulate echoes become visible. Echography is very helpful in evaluating eyes with dense vitreous haemorrhage in order to exclude the possibility of underlying retinal detachment (Fig. 17.1D) or retinal tear.

3Treatment varies according to the severity and underlying cause.

Table 17.1 -- Causes of vitreous haemorrhage

1Acute posterior vitreous detachment associated either with a retinal tear or avulsion of a peripheral vessel

2Proliferative retinopathies

•Diabetic

•Following retinal vein occlusion

•Sickle cell disease

•Eales disease

•Vasculitis

3Miscellaneous retinal disorders

•Macroaneurysm

•Telangiectasis

•Capillary haemangioma

4Trauma

•Blunt

•Penetrating

•Iatrogenic

5Systemic

•Bleeding disorders

•Terson syndrome

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